Through the smoke: Use of in vivo and in vitro cigarette smoking models to elucidate its effect on female fertility

Camlin, Nicole J.; McLaughlin, Eileen A.; Holt, Janet E.

doi:10.1016/j.taap.2014.10.010

Cited by 34 publications

(24 citation statements)

References 78 publications

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“…They act on the ovary via the aryl hydrocarbon receptor (AhR) present on the surface of granulosa cells. This receptor belongs to the family of transcription factors and activates the Bax gene, a pro-apoptosic gene, and the expression of cytochrome P450 that converts PAHs into even more toxic molecules [17, 62, 63]. Anderson et al have shown that activation of this receptor could lead to a decrease in germ cells in the ovary of the human fetus [64].…”

Section: Resultsmentioning

confidence: 99%

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Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

et al. 2017

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Background: Because only 25% of cases of premature ovarian insufficiency (POI) have a known etiology, the aim of this review was to summarize the associations and mechanisms of the impact of the environment on this pathology. Main body of the abstract: Eligible studies were selected from an electronic literature search from the PUBMED database from January 2000 to February 2016 and associated references in published studies. Search terms included ovary, follicle, oocyte, endocrine disruptor, environmental exposure, occupational exposure, environmental contaminant, pesticide, polyaromatic hydrocarbon, polychlorinated biphenyl PCB, phenol, bisphenol, flame retardant, phthalate, dioxin, phytoestrogen, tobacco, smoke, cigarette, cosmetic, xenobiotic. The literature search was conducted in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. We have included the human and animal studies corresponding to the terms and published in English. We have excluded articles that included results that did not concern ovarian pathology and those focused on ovarian cancer, polycystic ovary syndrome, endometriosis or precocious puberty. We have also excluded genetic, auto-immune or iatrogenic causes from our analysis. Finally, we have excluded animal data that does not concern mammals and studies based on results from in vitro culture. Data have been grouped according to the studied pollutants in order to synthetize their impact on follicular development and follicular atresia and the molecular pathways involved. Ninety-seven studies appeared to be eligible and were included in the present study, even though few directly address POI. Phthalates, bisphenol A, pesticides and tobacco were the most reported substances having a negative impact on ovarian function with an increased follicular depletion leading to an earlier age of menopause onset. These effects were found when exposure occured at different times throughout the lifetime from the prenatal to the adult period, possibly due to different mechanisms. The main mechanism seemed to be an increase in atresia of pre-antral follicles. Conclusion: Environmental pollutants are probably a cause of POI. Health officials and the general public must be aware of this environmental effect in order to implement individual and global preventive actions.

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Section: Resultsmentioning

confidence: 99%

“…According to the animal review from Camlin [62], cigarette smoking has negative effects on female fertility. Exposure to tobacco induces a depletion in follicle stock [75–78], according to a mechanism of apoptosis and oxidative stress [75–78].…”

Section: Resultsmentioning

confidence: 99%

Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

et al. 2017

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“…In animal models cigarette smoking leads to a depletion of primordial follicles (49), further loss of follicles throughout folliculogenesis, impaired cumulus oocyte complex expansion (361) and impaired granulosa cell function, granulosa cell steroid production, impaired oocyte meiosis (49), and a predisposition to aneuploidy within the oocyte (201). It is unclear how these translate for the woman that smokes cigarettes while attempting to conceive; however, it is known that smoking leads to a reduction in ovarian reserve and an advancement of the age of menopause for the woman (167,301), potentially due to the influence of polycyclic hydrocarbons which are activated into more toxic metabolites by the liver (49,271).…”

Section: Ovarian Functionmentioning

confidence: 99%

“…It is unclear how these translate for the woman that smokes cigarettes while attempting to conceive; however, it is known that smoking leads to a reduction in ovarian reserve and an advancement of the age of menopause for the woman (167,301), potentially due to the influence of polycyclic hydrocarbons which are activated into more toxic metabolites by the liver (49,271). Further human studies have demonstrated that oocytes derived from cigarette smoking women undergoing IVF treatment have a greater number of immature oocytes (385), an increased thickness of the zona pellucida (310), with follicles containing higher level of markers of oxidative stress within the follicular fluid (252), and within the cumulus (316).…”

Section: Ovarian Functionmentioning

confidence: 99%

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Hart

2016

Physiological Reviews

160

119

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Across the Western World there is an increasing trend to postpone childbearing. Consequently, the negative influence of age on oocyte quality may lead to a difficulty in conceiving for many couples. Furthermore, lifestyle factors may exacerbate a couple's difficulty in conceiving due mainly to the metabolic influence of obesity; however, the negative impacts of low peripheral body fat, excessive exercise, the increasing prevalence of sexually transmitted diseases, and smoking all have significant negative effects on fertility. Other factors that impede conception are the perceived increasing prevalence of the polycystic ovary syndrome, which is further exacerbated by obesity, and the presence of uterine fibroids and endometriosis (a progressive pelvic inflammatory disorder) which are more prevalent in older women. A tendency for an earlier sexual debut and to have more sexual partners has led to an increase in sexually transmitted diseases. In addition, there are several genetic influences that may limit the number of oocytes within the ovary; consequently, by postponing attempts at childbearing, a limitation of oocyte number may become evident, whereas in previous generations with earlier conception this potentially reduced reproductive life span did not manifest in infertility. Environmental influences on reproduction are under increasing scrutiny. Although firm evidence is lacking however, dioxin exposure may be linked to endometriosis, phthalate exposure may influence ovarian reserve, and bisphenol A may interfere with oocyte development and maturation. However, chemotherapy or radiotherapy is recognized to lead to ovarian damage and predispose the woman to ovarian failure.

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“…For example, a recent epidemiology study of women living within 4 kilometers of a municipal solid waste incinerator in Italy identified a significant increased risk for sPTB [79]. As noted previously, cigarette smoke is replete with a wide array of toxicants, including TCDD [80], and has long been associated with reduced fertility and low birthweight due to either primary or secondary exposures [81–83]. …”

Section: Environmental Endocrine Disruptorsmentioning

confidence: 99%

Exposure to the environmental endocrine disruptor TCDD and human reproductive dysfunction: Translating lessons from murine models

Bruner‐Tran

Gnecco

Ding

et al. 2017

Reproductive Toxicology

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Humans and other animals are exposed to a wide array of man-made toxicants, many of which act as endocrine disruptors that exhibit differential effects across the lifespan. In humans, while the impact of adult exposure is known for some compounds, the potential consequences of developmental exposure to endocrine disrupting chemicals (EDCs) is more difficult to ascertain. Animal studies have revealed that exposure to EDCs prior to puberty can lead to adult reproductive disease and dysfunction. Specifically, in adult female mice with an early life exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), we demonstrated a transgenerational occurrence of several reproductive diseases that have been linked to endometriosis in women. Herein, we review the evidence for TCDD-associated development of adult reproductive disease as well as known epigenetic alterations associated with TCDD and/or endometriosis. We will also introduce new “Organ-on-Chip” models which, combined with our established murine model, are expected to further enhance our ability to examine alterations in gene-environment interactions that lead to heritable disease.

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Through the smoke: Use of in vivo and in vitro cigarette smoking models to elucidate its effect on female fertility

Cited by 34 publications

References 78 publications

Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

Physiological Aspects of Female Fertility: Role of the Environment, Modern Lifestyle, and Genetics

Exposure to the environmental endocrine disruptor TCDD and human reproductive dysfunction: Translating lessons from murine models

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